Blood vessel reactivity on noradrenaline, vasopressin, and prostaglandin F2 alpha, resp., in the isolated perfused hind legs of rats with edemas or adjuvant arthritis.

In the isolated perfused hind legs of rats with enemas induced by carrageenin, dextran or Freund's adjuvant in both paws, resting perfusion pressure was slightly increased whereas the vasopressor action of noradrenaline, lysine-vasopressin and prostaglandin F2 alpha, was decreased. Admixture of indomethacin (3 micrograms.ml-1) to the perfusion fluid led to a decrease of resting perfusion pressure whereas its influence on EAmax of noradrenaline was only weak under these conditions. Concomitantly, the contents of prostaglandin E-like substances in the perfusate decreased. Prostaglandin F2 alpha exhibits only weak vasopressor activity in isolated perfused hind legs of rats with carrageenin edema. Altogether, the effect of indomethacin on resting perfusion pressure as well as on EA and EAmax, resp., of agonists is difficulty to explain by its effect on arachidonic acid cascade. The pD2-value of noradrenaline (4.68 - 4.87) and lysine-vasopressin (6.02 - 6.04) was apparently not changed, at least not decreased, in the acute phase of inflammation indicating no impairment of receptor affinity of noradrenaline and vasopressin in inflammation. Blood vessel reaction is apparently influenced in inflammation mechanically by the increased tissue pressure as well as by molecular mechanisms consisting in the presence of inflammatory mediators and/or particularly in a reduced intrinsic sensitivity of the blood vessel muscle itself.